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Left ventricular function in mice lacking the AT2 receptor.

V Gross1, T Walther, A F Milia

  • 1Franz Volhard Clinic and Max Delbrück Center for Molecular Medicine, Medical Faculty of the Charité, Humboldt University of Berlin, Germany.

Journal of Hypertension
|June 8, 2001
PubMed
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Mice lacking the angiotensin II type 2 receptor (AT2 receptor knockout mice) showed no significant changes in heart function. However, the AT2 receptor influences angiotensin II type 1 receptor expression and cardiac growth during deoxycorticosterone acetate-salt treatment.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Cardiology
  • Renal and Cardiovascular Pharmacology

Background:

  • The precise role of the angiotensin II type 2 receptor (AT2 receptor) in cardiac function remains incompletely elucidated.
  • Understanding its interplay with the angiotensin II type 1 receptor (AT1 receptor) is crucial for comprehending cardiovascular regulation.

Purpose of the Study:

  • To investigate the impact of AT2 receptor deficiency on left ventricular performance.
  • To examine the effects of deoxycorticosterone acetate (DOCA)-salt treatment on cardiac function in AT2 receptor knockout mice.
  • To analyze AT1 receptor expression in the context of AT2 receptor absence.

Main Methods:

  • Utilized a miniaturized conductance-manometer system to assess left ventricular pressure-volume loops.

Related Experiment Videos

  • Measured cardiac performance under baseline conditions and following increases in peripheral vascular resistance.
  • Quantified left ventricular AT1 receptor gene expression using RNase-protection assays.

    • Main Results:

    • AT2 receptor knockout mice exhibited altered ventricular volumes but comparable systolic and diastolic kinetics to wild-type mice.
    • DOCA-salt treatment increased elastance and dP/dtmax in AT2 receptor knockout mice.
    • Left ventricular AT1 receptor gene expression was elevated in knockout mice and unresponsive to DOCA-salt treatment; cardiac growth responses were also modulated.

    Conclusions:

    • Absence of the AT2 receptor did not cause major alterations in baseline or DOCA-salt-challenged left ventricular function.
    • The AT2 receptor appears to play a role in regulating AT1 receptor expression and cardiac growth under specific physiological challenges.